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Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo


Year of Publication:
Contact PI Name:
Greg M. Cole
Contact PI Affiliation:
Department of Medicine, UCLA, Los Angeles, California, USA
Fusheng Yang, Giselle P. Lim, Aynun N. Begum, Oliver J. Ubeda, Mychica R. Simmons, Surendra S. Ambegaokar, Pingping Chen, Rakez Kayed, Charles G. Glabe, Salley A. Frautschy
Primary Reference (PubMED ID):
Funding Source:
United States Department of Veterans Affairs (VA)
National Institute on Aging (NIA)
Alzheimer's Association
Siegel Life Foundation
National Institute of Neurological Disorders and Stroke (NINDS)
Study Goal and Principal Findings:

The overarching goal of this study was to test the hypothesis that curcumin (and other similar  polar Aβ binding compounds) might be able to cross the blood-brain barrier, bind to  and related aggregates, and inhibit beta amyloid fibril formation and beta amyloid plaque deposition.  In these studies the authors used an in vitro model of Aβ fibrillization to show that curcumin can bind amyloid to inhibit Aβ aggregation as well as fibril and oligomer formation with dosing at achievable levels.  In addition the authors demonstrated that curcumin can label plaques in vitro and in vivo, block toxicity of oligomers in vitro, and significantly reduce amyloid levels in aged Tg2576 mice (22 months old) fed a curcumin diet beginning at 17 months after established amyloid deposition. These data suggest that low dose curcumin effectively disaggregates Abeta as well as prevents fibril and oligomer formation and support the rationale for curcumin use in clinical trials preventing or treating AD.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Natural Product
Therapeutic Agent:
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Not Reported

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
beta Amyloid Load
beta Amyloid Aggregation
Brain-beta Amyloid Oligomers
Binding-beta Amyloid Fibrils
Cell Biology
Neuroprotection-Amyloid Neurotoxicity
Blood Brain Barrier Penetration
Target Engagement (Binding beta Amyloid Antibodies to beta Amyloid Deposits)